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Paediatrics > Y4 - Paediatric Diabetes > Flashcards

Y4 - Paediatric Diabetes Flashcards

1
Q

What are the types of diabetes that affect children?

A 
Type 1 (most common) 
Type 2
Monogenic diabetes (MODY)
Secondary diabetes, e.g. CF related diabetes
Neonatal diabetes (transient/persistent)
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2
Q

In which groups of people is T2DM more common?

A

Afro-Caribbean or Asian ethnicities

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3
Q

What causes MODY?

A

Autosomal dominant kind of non-ketotic diabetes in childhood/young adults
6+ causal genes exist
MODY is caused by SINGLE gene defects

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4
Q

What are the key features of MODY?

A

Diagnosed <25y
Having parent with DM with DM in two or more generations
Not necessarily needing insulin

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5
Q

What are the most common types of MODY gene mutations?

A

HNF-1a (70%)
HNF-4a
HNF-1b
Glucokinase

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6
Q

HNF1-a MODY (MODY3)

A

Defect on chromosome 12 that leads to progressive decrease in insulin production
Features severe hyperglycaemia after puberty
Diabetic retinopathy and nephropathy often occur
Rx: sulphonylureas

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7
Q

HNF4-a MODY

A

Generally Rx with SU but may progress to needing insulin

Rare

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8
Q

HNF1-b (MODY5)

A

Diabetes associated with renal cysts, uterine abnormalities, gout
Usually need insulin Rx

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9
Q

Glucokinase (MODY2)

A

No Rx required
Blood sugars usually only slightly elevated
Caused by mutation on glucokinase gene (chromosome 7)

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10
Q

What is the role of glucokinase?

A

Coverts glucose into glucose-6-phosphate, which is needed to stimulate insulin secretion from beta-cells

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11
Q

How does MODY differ from T1/T2DM?

A

Caused by a single gene, as opposed to T1/T2 which is caused by polygenic and environmental causes

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12
Q

Why is molecular diagnosis in MODY so important?

A

It has consequences for diagnosis, family screening & management

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13
Q

What does testing for MODY involve?

A

Having blood taken for pancreatic antibodies
Blood/urine tested for C-peptide
Blood for genetic testing

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14
Q

What does MODY stand for?

A

Maturity onset diabetes of the young

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15
Q

What is the pathogenesis of CF related diabetes?

A

Mutation of the CFTR gene leads to two things:
1. Increased infections (and release of inflammatory markers, e.g. TNF) and increased use of steroids leads to increased insulin resistance

  1. Thick secretions block the pancreatic duct –> fatty infiltration and fibrosis of pancreatic islet cells –> decreased insulin secretion

Both of these lead to hyperglycaemia

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16
Q

Describe the onset of CFRD

A

Gradual onset

Usually around 18-25y

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17
Q

In which patients is CFRD most common?

A

Those with homozygous Phe508del mutation of CFTR

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18
Q

How are children with CF screened for CFRD?

A

Annual screen for CFRD using OGTT by age 10 in patients with CF (without CFRD)

Annual review for complications after 5y of diagnosis of CFRD

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19
Q

How is CFRD treated?

A

Insulin

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20
Q

What is involved in the aetiology of T1DM?

A

Genetic susceptibility
Autoimmunity (T cell mediated destruction of pancreatic beta-cells)
Environment - i.e. viral trigger

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21
Q

What gene in particular is implicated in T1DM?

A

Insulin-dependent diabetes mellitus 1 gene locus

part of HLA DR/DQ locus on the major histocompatibility complex

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22
Q

How likely are you to get T1 diabetes if your identical twins has it?

A

50%

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23
Q

How likely are you to get T1 diabetes if your fraternal twin as it?

A

11%

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24
Q

Where is the incidence of T1DM highest? And why might this be significant?

A

UK, Finland, Sweden etc.

All on same latitude therefore may be correlation between vitamin D and T1DM

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25
Q

Describe the natural history of T1DM

A

Genetically susceptible individual is exposed to an environmental trigger
There is subclinical reduction in beta-cells
Symptoms appear after B-cell numbers have dropped significantly

(so there are several months after trigger where individual is symptom free)

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26
Q

What is the typical presentation of T1DM?

A 
Polyuria
Polydipsia
Weight loss
Fatigue
Abdominal pain (due to ketone build up)

DKA (around 25%)

27
Q

What factors make presentation of T1DM with DKA more common?

A 
Younger age
Diagnostic error 
Ethnic minority
Lower BMI
Preceding infection 
Lower socio-economic status
Unemployed mother
28
Q

What factors make presentation of T1DM with DKA less likely?

A

FH of T1DM
Higher parental education
Higher background incidence of T1DM
Presence of structured diabetes team

29
Q

What things are involved in managing the newly diagnosed T1 diabetic?

A

Advice re. exercise & health eating, insulin injections, hyperglycaemia and ketones, carb counting, glucose testing, hypos, insulin jumps, DKA

30
Q

Give examples of insulin regimens

A

Twice daily pre-mixed insulin
Basal bolus insulin
Carb counting
Insulin pump

31
Q

What does the twice daily pre-mixed insulin regimen involve?

A

Give starting dose of 0.5 units per kg
2/3 dose in morning pre-breakfast
1/3 dose pre-dinner
Adjusted according to blood glucose levels

32
Q

What does the basal bolus regimen involve?

A

Three doses of novorapid with breakfast, lunch & dinner

Long acting insulin at night before bed (e.g. Levemir)

33
Q

What must you educate parents about carb counting?

A

Identifying carbs in food
Calculating carbs in foods (labels, working out portion sizes etc.)
Teach insulin to carb ratios
How to correct if BG above target

34
Q

What does the insulin pump have to help with calculating doses?

A

Automated bolus calculator

35
Q

How does the pump give insulin?

A

Programmed background basal rate

Bolus doses

36
Q

Define hypoglycaemia

A

BG <4

37
Q

What are the symptoms of hypos?

A 
Anxiety/irritability
Shaking
Sweating
Tachycardia
Dizziness
Hunger
Blurred vision 
Weakness/fatigue
Headache
38
Q

How do you Rx a mild hypo?

A

Fast acting sugar (fruit juice, fizzy drinks, sweets, glucose tabs)
Recheck bloods in 10 minutes
If still <4 repeat dose of fast acting sugar

If >4 & <1h to next meal - no carbs; 1-2h to next meal take 10g carb; >2h to next meal take 20g carb

39
Q

How do you manage a moderate hypo where the child is unable to swallow?

A

Administer glucose gel into buccal mucosa

40
Q

How do you treat a severe hypo (child unconscious/fitting)?

A

IM glucagon

Call 999

41
Q

What does IM glucagon do?

A

Mobilises hepatic glucose

42
Q

What is the major SE of IM glucagon?

A

Severe vomiting

43
Q

How would you manage a severe hypo in hospital?

A

IV access - give glucose 5ml/kg 10% or by rectal tube if no IV access
With glucagon 0.5-1mg IM or slowly IV

Expect quick return to consciousness, if not recheck glucose, if low give dexamethasone IV

44
Q

If slow return to consciousness after severe hypo but normal BG now, what must you consider?

A

May have having post-ictal symptoms after a hypoglycaemic fit

45
Q

What are the symptoms of hyperglycaemia?

A 
Extreme thirst
Hunger
Polyuria
Dry skin 
Blurred vision 
Drowsy
Slow healing wounds
46
Q

What does DKA result from?

A

Deficiency of insulin and often increased levels of counter-regulatory hormones (e.g. catecholamines, glucagon, cortisol, growth hormone) e.g. due to sepsis

47
Q

What is the biggest concern with DKA in children (which is less common in adult DKA)?

A

Cerebral oedema

48
Q

What are other fatal events that can occur in DKAs?

A

Hypokalaemia

Aspiration pneumonia

49
Q

How do you prevent aspiration pneumonia in someone having a DKA?

A

NGT if semi-conscious to protect airway

50
Q

What are the clinical features of DKA?

A 
Listlessness
Confusion 
Vomiting
Polyuria
Polydypsia
Weight loss
Abdominal pain 
Dehydration 
Kussmaul breathing
Pear drop breath 
Shock 
Drowsiness 
Coma
51
Q

When should you check for ketones?

A

If BG is >15mmol/l

52
Q

What is kussmaul breathing?

A

Deep and laboured breathing in an attempt to reduce CO2 in the blood

53
Q

What are the 6 things patients are told to look out for in DKA?

A 
Persistent vomiting >4h
Heavy or rapid breathing
Abdominal pain 
Moderate/severe dehydration 
High BG (>17)
54
Q

What is the triad of DKA required for diagnosis?

A 
Hyperglycaemia (11mmol/L+)
Acidosis 
- Mild pH <7.3
- Mod pH <7.2
- Severe pH <7.1
Ketones (in urine/blood)
55
Q

How do you manage DKA?

A

ABC
If shocked give fluid bolus 10mls/kg & reassess
IV fluids (normal saline & KCl)
Start insulin infusion 1-2h after fluid starts

56
Q

What is your aim for DKA management?

A

Slow drop in BG of 5mmols/hour

Start insulin at 0.1u/kg/h

57
Q

What Ix do you want to do in DKA?

A 
Hourly BG
2-4hrly blood gases and electrolytes
Hourly neuro obs (cerebral oedema risk)
May want to do ECG 
Weighing 
Infection screen (sepsis may cause DKA)
58
Q

What must children with T1DM always carry around with them?

A

Blood sugar meter and hypo kit

59
Q

What is HbA1c?

A

Glycosylated haemoglobin
Gives an idea of BG control over lifespan of a RBC (120 days)
Higher HbA1c correlates with higher incidence of diabetic complications

60
Q

When should you stop giving insulin in a patient with DKA?

A

Once blood ketone levels <1 & patient able to tolerate food
Give s/c insulin, feed patient
Stop insulin infusion 10-60m after s/c insulin injection

61
Q

What symptoms may indicate cerebral oedema?

A

Headache or behaviour change

62
Q

In which people is cerebral oedema most common?

A

In children

Especially those who have had a rapid fall in glucose or sodium

63
Q

What should you do if you suspect infection in DKA?

A

MSU, blood culture, CXR

Start BS antibiotics

Paediatrics (35 decks)

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